Each year over a million patients in the US are treated with vascular surgical procedures for flow-limiting atherosclerosis or for hemodialysis access. Although initially successful, a large proportion of these reconstructions eventually fail due to intimal hyperplasia (IH). IH can result from injury that occurs at the time of arterial reconstruction, for example, manipulation of a vein being prepared for bypass. Alterations of hemodynamics can provide a more persistent stimulus for IH. An example of this is the exposure of a vein graft to arterial pressures and subsequent arteriolization of the vein. The development of recurrent disease leads to the narrowing of the new conduit with the eventual development of stenosis or occlusion.
IH remains a major cause of poor patient outcomes after surgical revascularization to treat atherosclerosis. A multitude of drugs have been shown to prevent the development of IH. Moreover, endovascular drug delivery following angioplasty and stenting has been achieved with a marked diminution in the incidence of restenosis. Despite advances in endovascular drug delivery, there is currently no clinically available method of periadventitial drug delivery suitable for open vascular reconstructions.